title: Genomic background-related activation of microglia and reduced β-amyloidosis in a mouse model of Alzheimer's disease.
abstract: Alzheimer's disease (AD) is by far the most common neurodegenerative disease. AD is histologically characterized not only by extracellular senile plaques and vascular deposits consisting of β-amyloid (Aβ) but also by accompanying neuroinflammatory processes involving the brain's microglia. The importance of the microglia is still in controversial discussion, which currently favors a protective function in disease progression. Recent findings by different research groups highlighted the importance of strain-specific and mitochondria-specific genomic variations in mouse models of cerebral β-amyloidosis. Here, we want to summarize our previously presented data and add new results that draw attention towards the consideration of strain-specific genomic alterations in the setting of APP transgenes. We present data from APP-transgenic mice in commonly used C57Bl/6J and FVB/N genomic backgrounds and show a direct influence on the kinetics of Aβ deposition and the activity of resident microglia. Plaque size, plaque deposition rate and the total amount of Aβ are highest in C57Bl/6J mice as compared to the FVB/N genomic background, which can be explained at least partially by a reduced microglia activity towards amyloid deposits in the C57BL/6J strain.
authors.affiliation: Neurodegeneration Research Lab (NRL), Department of Neurology, University of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany.
authors.forename: Christina
authors.initials: C
authors.lastname: Fröhlich
authors.forename: Kristin
authors.initials: K
authors.lastname: Paarmann
authors.forename: Johannes
authors.initials: J
authors.lastname: Steffen
authors.forename: Jan
authors.initials: J
authors.lastname: Stenzel
authors.forename: Markus
authors.initials: M
authors.lastname: Krohn
authors.forename: Hans-Jochen
authors.initials: HJ
authors.lastname: Heinze
authors.forename: Jens
authors.initials: J
authors.lastname: Pahnke
keywords: Alzheimer’s disease; genomic background; microglia; mouse models; neurodegeneration; neuroinflammation